PET imaging of human brain gliosis using Imidazoline2 (I2) binding sites: potential biomarker for Alzheimer's disease
PET imaging of human brain gliosis using Imidazoline2 (I2) binding sites: potential biomarker for Alzheimer's disease
批准号:
G0801501/1
负责人:
David Nutt
金额:
$60.01万
依托单位:
依托单位国家:
英国
项目类别:
Research Grant
财政年份:
2009
资助国家:
英国
项目状态:
已结题
起止时间:
2009 至 --
中文摘要
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英文摘要
Illnesses that affect the brain such as dementia cost the NHS and the country tens of billions of pounds and are the main cause of disability in old people. In a recent report for the Alzheimer?s Society it was estimated that dementia as a whole costs the country #17.03 billion per year, or an average of #25,472 per person with dementia. Nearly 700,000 people have dementia in the UK, of which 434,000 have Alzheimer?s disease (AD). There are other brain illnesses that are less common and less costly but still very painful to the people that have them and their relatives, such as multiple sclerosis (MS) and brain tumours. One of the things these illnesses have in common is inflammation within the brain. If we were able to measure this inflammation in living humans, it would enable us better to diagnose these illnesses at an early stage when we have the best chance to cure or slow down their development. Being able to measure this inflammation will also enable us to monitor and understand these illnesses better, and any potential treatments. The purpose of this work is to develop a way of measuring this inflammation using Alzheimer?s disease as a model. The way we intend to do this is to use a very powerful technique for visualising inside humans, called positron emission tomography, or PET. PET relies on specially designed radioactive chemicals that provide a means to visualise what is happening in the brain. Therefore, we plan to develop such a radioactive chemical for a protein called the imidazoline2 binding site. This protein is found in a type of brain cell called glial. These cells are a normal part of the brain. However, in the illnesses such as Alzheimer?s where the brain is damaged and inflammation exists, there are more of these cells, especially in the inflamed areas. We already know that the amount of this protein is increased in the brains of people who have died of Alzheimer?s by studying post-mortem tissue. If we can measure a change in this protein in living patients with Alzheimer?s, it will mean we have a way of measuring this brain inflammation found in this and similar illnesses, early on giving the sufferer the best chance.
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